HAEMOPHILIC ARTHROPATHY: IMMUNOLOGICAL MECHANISMS AND SYNOVITIS

Up to now questions of pathogenisis in hemophilic arthropathy are still remaining, i.e. humoral mediated imnunological mechanisms (type II/III reactions) are supposed to play an important role (Arnold and Hilgartner (1977), Rippjey (1978)). Therefore we investigated synovial tissue by imnunohistologic technique using antibodies against IgG, IgA, IgM, C1q, C3, fibrinogen ando61-ACT. First we examined synovial membrane biopsies (n=7; non-haemo-philic) following acute traumatic joint bleeding, to study the first and acute bleeding/absorption pahase. Light microscopy showed typical changes as described before by Roy et al. 1967. Iirrnunohistological results revealed negativity for immunoglobulins and complement components in general, whereas fibrinogen and α1-ACT showed marked intensity of fluorescence.

Secondly synovial membrane biopsies (n=7) of haemophiliacs who have had recurrent joint bleedings were examined, in the same way. In light microscopy we found typical synovial alterations as described by Mohr (1984) . Immunohistology shewed negativity for immunoglobulins and complement components and the intensity of fluorescence of fibrinogen and α1 -ACT was lower as in patients with acute traumatic joint bleeding.

At last synovial tissue specimens (n=2) of patients with pigmented villonodular synovitis were investigated. Light microscopy was in aquaintance with findings of FaBbender (1976) . The imnuno-histological results were similar to those aforementioned. Conclusions: 1) There is no evidence that acute or chronic joint bleeding causes a humoral mediated immune reaction in synovial membrane. 2) In the contrary the inflammatory reaction leeds to detritus-synovialitis, supported by recurrent bleeding episodes. Concequences for clinical management: a) prevention of joint bleeding b) joint-pxinction in cause of bleeding, to reduce the intraarticular haematcma c) synovectomy to prevent the progress of arthropathy.